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Query: UMLS:C0014547 (focal epilepsy)
 1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonketotic hyperglycemia has a definite convulsive effect, which may manifest itself in generalized or focal seizures. This report deals specifically with focal convulsive phenomena. Two patients with nonketotic hyperglycemia focal seizures are described. Focal seizures are of motor Jackson, aphasic, adversive or of the 'epilepsia partialis continua' type. Different types of focal seizures may appear in one and the same patient. Focal epilepsy can be the first manifestation of a diabetic disorder. Focal epileptic seizures are linked with moderate nonketotic hyperglycemia with values of 360 mg% sugar and 310 osm. Higher values lead to generalized seizures and coma. The mechanisms are discussed and pertinent literature is reviewed.
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PMID:Moderate nonketotic hyperglycemia--a cause of focal epilepsy. Report of two cases and review of literature. 9 31

This report is a sequel to our 1958, 1960 and 1968 reports on a series of patients operated upon for focal epilepsy whose surgical specimens unexpectedly showed histological lesions typical of active encephalitis. None of these patients, now 27 in number, exhibited the clinical picture ordinarily associated with encephalitis. With one exception, all showed a severe focal seizure tendency beginning in infancy or childhood, often associated with episodes of epilepsia partialis continua. In addition, all except 2 showed slowly progressive neurological deterioration, usually hemiparesis and mental retardation, which advanced over periods of months or years before the progression became arrested. No infectious agent has yet been identified by standard viral studies carried out in the most recent 14 patients or by investigation for slow viruses in 6 patients operated upon between 1966 and 1971. The clinical course of this condition is outlined and the role, the timing and the results of treatment by craniotomy and cortical excision are discussed.
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PMID:Further observations on the syndrome of chronic encephalitis and epilepsy. 10 97

The author reports the discovery of an original entity, the activated astrocyte, which is an essential component and the first anatomical sign of the epileptogenic focus. The importance of the activated astrocyte is demonstrated by the fact that it is observed before the clinical signs appear and as soon as the first spikes are recorded on the electrocortigram. Cautious conclusions are drawn. The authors recognizes the essential role of the neurons and does not suggest that astrocytes are the cause of epilepsy. However, since astrocyte activation is observed before the first electrical signs announce the beginning of an epileptogenic focus, he suggests that activated astrocytes probably offer morphological evidence of certain mechanisms closely concerned in the formation of the epileptogenic focus. The metabolic activation of the astrocyte is not surprising, and is probably related to the increase in loco-regional metabolism due to neuronal hyperactivity, the starting point of epilepsy. It confirms current opinion, especially in biochemistry, on the importance of the glial cells in the neuronastrocyte association. This work opens up certain prospects. First, the significance of the activated astrocyte in the context of current biochemical, neuro-physiological and morphological studies of the glial compartment is a promising research field. Second, from the clinical angle, it is very important to be able to identify an epileptogenic gliosis on the basis of activated astrocytes. Used in conjunction with modern neuro-physiological techniques to locate the epileptogenic focus, the search for activated astrocytes in biopsy material obtained stereotactically should permit better detection of the affected area and thus ensure more successful surgery in cases of focal epilepsy resistant to medication.
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PMID:[Activated astrocytes and epileptogenic focus. Histoenzymology]. 38 3

Sodium valproate (Epilim) has been used in the management of 100 patients with previously uncontrolled epilepsy for periods up to 2 years. If all manifestations of epilepsy are considered together, 75% to 100% control of seizures was achieved in 43% of patients, 25% to 74% control in 26%, and no improvement occurred in 31% of patients. Control of 75% to 100% was achieved in 57% of patients with a spike and wave electroencephalogram (EEG) disturbance but only in 35% of those with focal abnormalities, excessive slow activity, or normal records. When the various manifestations of epilepsy were considered individually, the greatest improvement was found among the patients with the minor forms of generalized epilepsy (petit mal absences, myoclonus and atonic attacks) in whom 75% to 100% control was obtained in 67%, compared with 43% of those with major generalized seizures (grand mal) and 30% of those with temporal lobe attacks and other forms of focal epilepsy. Gastrointestinal disturbances and drowsiness were noted as side effects in the early stages of treatment, but the majority of patients tolerated the drug well and many commented on increased mental alertness while taking it. Two patients were over-stimulated and some noticed tremor or twitching as side effects. Some minor abnormalities in blood coagulation studies were noted, but these were transient and did not appear to be of clinical significance. Regular blood counts and biochemical studies have not shown any significant changes. Sodium valproate appears to be a safe and useful anticonvulsant with the advantage that it usually makes patients brighter rather than drowsier. Abnormalities of platelet function have been described in some overseas reports, so that any unexplained bruising or bleeding in a patient taking valproate is an indication for a platelet count and coagulation studies.
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PMID:The anticonvulsant action of sodium valproate (Epilim) in 100 patients with various forms of epilepsy. 40 31

For activation of electrocorticographic records the authors administered intravenously thiopental or Brietal to 86 patients undergoing operations for various types of focal epilepsy. Thiopental was administered either in intravenous drip infusion as 0.2% solution, or in a single injection of 2.5% solution. Brietal was injected as 1% solution intravenously. Thiopental activated electrocorticographic tracings in 56.3% and Brietal in 84% of the patients. In the conclusions the authors stress that both these agents may be used for activation of pathological discharges in ECoG in patients with epilepsy operated upon under general anaesthesia. Brietal seems to be better and it may be administered many times.
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PMID:[Comparison between thiopental and brietal in the activation electrocorticographic records in epileptics]. 40 22

The controversial relations between migraine and vascular headache on one hand, epilepsy on the other hand are once more discussed: survey of the arguments for a more than fortuitous connexion, taken from literature and general experience. Critical analysis of the personal case material. Discussion of some specific groups of patients with various combinations of both syndromes: long antecedents of headaches, leading up to sporadic epileptic attacks, focal or generalized; clinical seizures under photic stimulation (10% of the cases with chronic headaches without organic lesions); headaches in the latency period of symptomatic epilepsy; cases of seeming transition between the two syndromes; headaches as a substitute, an aura or as a component of the epileptic seizure, with clearly distinctive features between generalized and focal epilepsy: in patients with bilateral EEG paroxysms, headaches are usually diffuse or bilateral, in those with epileptogenic foci, headaches, if consistently localized, are always reported to be homolateral to the focus. Considerations concerning pathogenesis include the familiar hypothesis of hypoxic discharges following migrainous vasoconstriction, as well as secondary vascular headaches induced by focal epileptic activity. Headaches caused by excessive discharges in the sensory representation areas (H. Jackson) must be rare. Whether increased neuronal activity in the hypothalamus may be responsible for the migraine syndrome (Herberg), possibly in connection with biogenic amines, remains in open question.
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PMID:[Epilepsy and headaches (author's transl)]. 41 Jun 25

The present prospective study undertaken in a specialized neurological center of a developing country deals with 1,000 epileptic patients classified in accordance with the International Classification. Eighty-one percent of the patients could be classified, with a lower incidence in the younger age group. Partial epilepsy was found to be far more common than generalized epilepsy (80% versus 20%). Primary generalized epilepsy was seen in 15% and secondary generalized in 5%. Partial epilepsy with elementary symptomatology was seen in 58% and complex symptomatology in 7%. Secondarily generalized seizures were seen in the remaining 15%. Primary generalized epilepsy and partial epilepsy with complex symptomatology were more common in adults. Secondary generalized epilepsy and partial epilepsy with secondarily generalized seizures were more common in children. Partial epilepsy with elementary symptomatology, however, did not vary significantly with age. The higher incidence of partial epilepsy in our patients, compared to the West, could be due to greater frequency of CNS infections and birth injuries, which are common childhood hazards in the developing countries.
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PMID:Profile of epilepsy in a developing country: a study of 1,000 patients based on the international classification. 41 69

Free amino compounds were measured in 16 rapidly frozen epileptogenic foci excised from temporal or frontal cortex of nine patients with focal epilepsy, and in single cortical biopsy specimens obtained from 16 nonepileptic patients. Unlike the findings of a previous study, glutamic and aspartic acids were not diminished in the foci, nor was there a decrease in gamma-aminobutyric acid (GABA) or taurine levels. Glycine content was markedly elevated in two of 16 epileptogenic foci. These results do not suggest that deficiencies of GABA or of taurine, amino acids that may act physiologically as inhibitory neurotransmitters or modulators of inhibition, are causes of focal epilepsy, nor do they provide a logical basis for clinical trials of taurine in treatment of human epilepsy.
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PMID:Amino acids in human epileptogenic foci. 81 Jan 20

Among the 1100 patients with convulsive disorders attending out-patient paediatric clinics of the Universities of Vienna and Graz, there are 14 cases of postnatal posttraumatic epilepsy. The characteristic features of this condition, as evidenced even by this small group of patients are focal epilepsy with focal paroxysms in the EEG, often combined with neurological defects and psychological abnormalities, but more seldom with defects of intelligence; resistance to anticonvulsive drugs is a frequent observation. In a retrospective study such as this, the criteria which could predict the development of epilepsy following posttraumatic brain damage are not sufficiently accurately definable; prospective serial studies on brain-damaged children would be of greater prognostic value. The following parameters seem to be important: the kind of brain damage, the duration of unconsciousness, the frequency of initial convulsive attacks and the persistance of the progression of the EEG changes.
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PMID:[Brain damage and epilepsy in childhood (author's transl)]. 81 91

Between 3700 and 3900 children are admitted annually to this children's hospital. During the past four years a total of 455 children with convulsions were admitted for investigation. 255 of these cases were calcified as epilepsy, 202 as febrile convulsions and 28 as neonatal convulsions. A quarter of the epileptic children showed fits of the petit mal type. There were only 5 cases of infantile propulsive petit mal. High frequency of fits and, in particular, status epilepticus, were very rarely seen in the present study. A case of self-induced photosensitive epilepsy, later combined with psychomotor epilepsy, is referred to in detail. Of 149 children with grand mal epilepsy, 36 were classed as idiopathic, and 88 as symptomatic cases. 37 of the symptomatic cases showed focal epilepsy with generalisation. It was concluded from the clinical course and the EEG that the combined effects of familial predisposition towards fits and exogenous cerebral lesions were operative factors in 14 patients. Children with febrile, convulsions possessed an EEG suggestive of a familial predisposition towards fits in slightly more than 50% of the cases. No cause could be found for the seizures in 5 infants with neonatal convulsions, but the mother of one of these infants was an epileptic herself, undergoing treatment with anticonvulsive drugs in high dosage and a withdrawal syndrome was suspected in this particular case. 17 infants with neonatal convulsions were symptomless on leaving hospital and remained so during the first year of life. Of the remaining cases, 10 showed neurological disturbances and one died. There was only one case in which neonatal convulsions progressed directly to epilepsy. The peak incidence of the first appearance of fits occurred during the first year of life (136 children), with 18% of the entire case material presenting within the first 6 months. 108 children presented with fits for the first time during the second year of life. Thereafter, the tendency towards the development of fits for the first time in life declined with increasing age.
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PMID:[Aspects of epilepsy in childhood (author's transl)]. 81 19


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